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The Pat1-Lsm complex prevents 3 to 5 degradation of a specific subset of ATG mRNAs during nitrogen starvation-induced autophagy

机译:Pat1-LSM复合物在氮气饥饿诱导的自噬期间防止3至5次特定子集的特定子集的降解

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摘要

Deregulation of macroautophagy/autophagy, a conserved catabolic recycling pathway, has been implicated in the onset and development of several diseases. While post-translational regulation of auto-phagy-related (Atg) proteins has been an important research focus leading to significant breakthroughs in understanding autophagy regulation, less is known about the post-transcriptional regulation of ATG transcripts. In a recent study we showed that, during nitrogen starvation, the RNA-binding complex Pat1-Lsm is involved in binding and preventing the 3' to 5' exosome-mediated degradation of a specific subset of ATG mRNAs. Dephosphorylation of Pat1 at residues S456 and S457 facilitates ATG mRNA binding, resulting in ATG mRNA accumulation, Atg protein synthesis and robust autophagy induction. In addition, we present evidence that these processes are conserved in human cells. These results further elucidate our understanding of the post-transcriptional mechanism necessary for efficient induction of autophagy during stress conditions.
机译:对巨噬细胞/自噬的放松管制,一种保守的分解代谢再循环途径,已涉及几种疾病的发作和发育。虽然自动吞噬(ATG)蛋白质的翻译后调节是一个重要的研究重点,但在了解自噬条例方面的重大突破,较少关于ATG转录物的转录后调节。在最近的一项研究中,我们表明,在氮饥饿期间,RNA结合复合Pat1-LSM涉及结合和预防3'至5'外介导的ATG MRNA的特定子集的介导的降解。在残基S456和S457处的Pat1的去磷酸化有助于ATG mRNA结合,导致ATG mRNA积累,ATG蛋白质合成和鲁棒自噬诱导。此外,我们提出了这些过程在人体细胞中保存的证据。这些结果进一步阐明了我们对在应激条件下有效诱导自噬所必需的转录后机制的理解。

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